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Biomedical subjects

S Nagaya

Publications and source records attributed to S Nagaya.

32 records · Page 2Linked to original sources
PubMed1995

[Acute promyelocytic leukemia following ulcerative colitis].

We report a case of acute promyelocytic leukemia (APL) following ulcerative colitis (UC). A 23-year-old man was diagnosed as UC in January 1991 and had been treated with salazosulfapyridine and prednisolone with good effect. In September 1993, he developed bleeding tendency and a diagnosis of APL with disseminated intravascular coagulation was made based on the results of bone marrow aspiration and coagulation profile. Complete remission was achieved with All-trans retinoic acid together with combined chemotherapy. He died of sepsis during consolidation chemotherapy in December 1993. Autopsy revealed no recurrence of UC.

Adult↗
PubMed1995

Decreased plasma tissue factor pathway inhibitor levels in patients with thrombotic thrombocytopenic purpura.

We measured plasma levels of tissue factor (TF) and tissue factor pathway inhibitor (TFPI) in patients with thrombotic thrombocytopenic purpura (TTP) and disseminated intravascular coagulation (DIC) to examine the relationship between TFPI and vascular endothelial cell injury. TF antigen was detected in the plasma of healthy volunteers, and the levels were significantly increased in the patients with DIC, but decreased slightly in those with TTP. Plasma TFPI levels were significantly decreased in patients with TTP compared with those in healthy volunteers. The concentration of plasma thrombomodulin (TM) antigen was significantly higher in those with TTP than in normal volunteers. One month after treatment, TTP patients showed a significant decrease in plasma TM levels, and a significant increase in plasma TFPI levels, but plasma levels of TF antigen were not significantly increased. As plasma TFPI/TF ratio was significantly increased after treatment, the hypercoagulable state was therefore improved after treatment. There was no significant difference in plasma TF and TFPI levels between those who achieved complete remission (CR) and those who died. However, plasma TM levels were significantly higher in those who died than in those who achieved CR. Plasma TFPI levels might reflect injury of vascular endothelial cells as do plasma TM levels, and decreased plasma TFPI/TF ratio and vascular endothelial cell injuries might play causative roles in TTP.

Adolescent↗
PubMed1995

Outcome of disseminated intravascular coagulation in relation to the score when treatment was begun. Mie DIC Study Group.

We examined 395 patients with disseminated intravascular coagulation (DIC) divided into two groups: non-leukemic and leukemic. In 58% of the patients as a whole, treatment of DIC resulted in complete or partial remission, while exacerbation and death occurred in 31%. The efficacy of DIC treatment in the non-leukemic group was less than that in the leukemic group, indicating that the outcome of DIC depended, in part, on the underlying disease. We examined hemostatic indicators in relation to DIC score: prothrombin time (PT) ratio, FDP, platelet count, and fibrinogen levels were found to be important indicators for the diagnosis of DIC, but not for Pre-DIC. Plasma levels of fibrin-D-dimer, thrombin-antithrombin complex (TAT), and plasmin-plasmin inhibitor complex (PPIC) were significantly increased in pre-DIC. The efficacy of treatment in relation to the DIC score when the treatment was begun showed that greater efficacy was achieved in pre-DIC than in DIC patients. The outcome was poorer with increasing DIC score, suggesting that early diagnosis and early treatment are important. On examining the relationship between outcome and hemostatic indicators, we found that the PT ratio and the levels of antithrombin, plasminogen, PPIC, the PPIC/TAT ratio, and thrombomodulin were related to outcome, suggesting that very high consumption of blood coagulation factors, liver dysfunction, hypofibrinolysis, or organ failure caused a poor outcome. Although the outcome in DIC patients may not depend substantially on plasma levels of TAT and fibrin-D-dimer, we can use these indicators to treat DIC patients at an early stage.

Antifibrinolytic Agents↗
PubMed1994

Effect of lipoproteins on tissue factor activity and PAI-II antigen in human monocytes and macrophages.

Expression of the tissue factor (TF) and the plasminogen activator inhibitor-II were induced in cultured human monocytes-macrophages by incubation with lipoproteins. Very low-density lipoprotein (VLDL) augmented the TF and PAI-II expression the most, followed by low-density lipoprotein (LDL) and a very weak effect by high-density lipoprotein (HDL). In macrophages pre-cultured for 3 days, oxidized LDL augmented the expression of TF activity in the macrophages to a greater extent than native LDL. These findings indicate that lipoproteins affect both monocytes and macrophages, and that they induce a hypercoagulable-hypofibrinolytic state. Thus hyperlipidemia may be a direct risk factor for thrombotic disease.

Blood Coagulation↗
PubMed1994

Increased vascular endothelial cell markers in patients with chronic renal failure on maintenance haemodialysis.

Plasma levels of the vascular endothelial cell markers, thrombomodulin (TM), plasminogen activator inhibitor-1 (PAI-1), tissue type plasminogen activator (t-PA), and von Willebrand factor (vWF) were measured in 55 patients on maintenance haemodialysis (HD). TM, PAI-1 and vWF antigen levels were significantly increased in patients before HD, but t-PA antigen was not Compared with levels before HD, t-PA and vWF antigens were significantly increased 1 h after HD and at the end of HD. TM antigen was significantly increased 1 h after HD, and plasma PAI-1 antigen was decreased at the end of HD. TM and vWF antigen levels were negatively correlated with the time (years) on HD. It is concluded that HD may cause endothelial cell damage and that the increases in plasma TM, PAI-1 and vWF levels before HD, and the decrease in the release of TM and vWF antigens from vascular endothelial cells, might be caused by vascular endothelial cell damage from long-term HD.

Adult↗
PubMed1994

Quadruple cancers in a human T-cell leukemia virus type 1 carrier.

Human T-cell leukemia virus type 1 (HTLV-1) infection is considered to contribute to the risk of malignancies other than adult T-cell leukemia. We report a 64-year-old male HTLV-1 carrier who developed quadruple malignancies such as cancer of the urinary bladder, skin, larynx and liver.

Basal Cell Carcinoma↗
PubMedDate not supplied

Metabolic engineering of cultured tobacco cells.

Construction of a gene expression system in tobacco cultured cells (BY2) was studied. A 925 bp promoter fragment of a heat-shock protein gene (HSP18.2) of Arabidopsis thaliana showed clear heat-shock response of expression of the beta-glucuronidase (GUS) reporter gene in BY2 cells. Similar results were observed in a 500 mL flask and 3-L jar fermentor. Isolation of strong promoters in BY2 cells was tried. cDNA clones, in which the mRNA level is high in log-phase cells and the copy number in the genome is low, were isolated. These clones showed high homology with F1-ATPase (mitochondria type), elongation factor 1-alpha, and a gene with an unknown function of A. thaliana (clone 27), respectively. A 5'-flanking region of clone 27 showed 6.2 times the promoter activity of the CaMV35S promoter in BY2 cells. Three cDNA clones, which are expressed in the stationary growth phase of BY2 cells, were isolated by a differential screening. These clones showed high sequence homologies to alcohol dehydrogenase, pectin esterase, and extensin. Promoters of these genes will be useful in gene expression in high cell-density culture.

Alcohol Dehydrogenase↗
PubMedDate not supplied

Diagnosis of pre-disseminated intravascular coagulation stage with hemostatic molecular markers. The Mie DIC Study Group.

We examined various hemostatic abnormalities in 395 patients with disseminated intravascular coagulation (DIC), in 177 patients in a Pre-DIC stage, and in 99 patients who did not exhibit DIC. Pre-DIC was defined as the condition at least one week before the onset of DIC. The differences in activated partial thromboplastin time (APTT), FDP, prothrombin time (PT) ratio, fibrinogen, and platelet count between DIC and Non-DIC patients were significant, but there were no significant differences in these parameters between Pre-DIC and Non-DIC patients. Plasma levels of fibrin-D-dimer, thrombin-antithrombin complex (TAT), plasmin-plasmin inhibitor complex (PPIC), soluble fibrin monomer (sFM), prothrombin activated peptide F1 + 2 (F1 + 2), thrombomodulin (TM), tissue type plasminogen activator (t-PA), and PA inhibitor (PAI-I) in DIC patients were significantly higher than levels in Non-DIC patients. However, only TAT, sFM and PAI-I values in the Pre-DIC patients were significantly higher than the values in the Non-DIC patients. Almost all the hemostatic molecular markers examined had high sensitivity for DIC, but only TAT and PPIC had high sensitivity for Pre-DIC. Specificity for DIC was also high with TAT, sFM, and F1 + 2. Early diagnosis and early treatment are important in DIC; we believe that it is possible to predict Pre-DIC by assessing values for the combination of hemostatic molecular markers.

Antithrombin III↗